Compensated myocardial hypertrophy occurring in response to chronic pressure overload usually progress to a decompensated state, with myocardial depression and cardiac pump dysfunction. The mechanisms involved in the transition from the chronically adapted to the chronically failing heart remain unclear. A major reason has been a relative lack of animal models of stable hypertrophy. We have developed a practical and reproducible model of cardiac hypertrophy that progresses to chronic heart failure, within three months, by banding the ascending aorta of young rats. Gradual left ventricular overload occurs as the animals mature, leading to a compensated left ventricular hypertrophy and subsequent cardiac failure. Animals with cardiac failure, identified by clinical symptoms (increased respiratory rate), presented pathophysiological alterations consistent with heart failure: high lung weight, hypertrophy of the left atria, right ventricle, and right atria. In addition most of the failure animals were observed to have pleural effusions. The first physiological study on animals provided by our experimental model show that the contractile behavior of myocytes isolated from failing hearts tended to be different under stressful conditions. Myocytes from failing hearts had reduced rates of twitch shortening and rates of relenghthening, especially at high drive rates (2.5 Hz) or at elevated external calcium concentrations (6 mM), compared to control. Application of the different technology available in the laboratory, such as measures of intracellular calcium handling with Indo-1, molecular biology ..., to this model of progressive heart failure should be able to elucidate mechanisms that underlie the transition from compensated hypertrophy to chronic heart failure.